As I understand it, the membrane of LDL contains polyunsaturated fatty acids (PUFA), which are highly vulnerable to oxidation. This oxidation, due to poor LDL receptor activity, lack of antioxidants or otherwise, is what causes atherosclerotic plaque to form.
PUFAs are very delicate and prone to oxidation unlike saturated fats which are more stable.
So, by minimizing our intake of PUFAs, is that reducing possible oxidation of LDL? That would imply that the fatty acid profile of the LDL membrane would change?
or is it reducing oxidative damage only in other places and not really effecting oxidized LDL?
asked byJeff__1 (15236)
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on December 17, 2011
at 03:31 AM
im surprised that this traditional dogma is on a paleo site. we have this wonderful mechanism to prevent death due to bleeding called atherosclerosis that was selected for when humans or some lessor creature lost the ability to form vitamin C and couldn't make collagen in its absence. its a stop gap mechanism. the topic of atherosclerosis is not even remotely related to cholesterol or oxidative processes or dietary fats. the human species is under chronic scurvey. i read just yesterday that 30 percent of americans have gingivitis. just look at the treatment for gingivitis just take vitamin c and it goes away.
on November 27, 2011
at 06:14 PM
there is an interesting recent study on the o3 vs. o6 content of LDL and health - was released a few weeks ago... I will have to dig that up again. Its in the queue for next weeks SuppVersity news, anyways.
ok, I dug it up
Quantification of the major ω-3, ω-6 PUFAs using the Purdie assay and their ratios in different cholesterol types and the effects of gender and cholesterol on PUFA levels Mary Muriuki, Neil Purdie, Gerard Dumancas This study used the Purdie assay, a new assay, to quantify the levels of omega-3 (ω-3) and omega-6 (ω-6) polyunsaturated fatty acids (PUFAs) in mol/L and the ratio of ω-6:ω-3 in total cholesterol (TC), high-density lipoprotein cholesterol, (HDL-C) and low-density lipoprotein cholesterol (LDL-C) (referred to throughout as “non-HDL-C” in this study) fractions in 35 samples of human serum and also assessed the influence of gender and cholesterol types on levels of the analyzed PUFAs. Three principal components explained 89% of the total variance based on the variables measured. The ratio of ω-6:ω-3 PUFAs was significantly influenced by the type of cholesterol (F = 10.84, df = 2, 99, P = < 0.001) but not gender or interaction between gender and type of cholesterol, while the total PUFAs and the levels of ω-3 and ω-6 PUFAs were significantly influenced by gender, but age did not have a significant effect on the levels for total PUFAs. The findings of this study imply that, for males, more focus should be on the ratios of ω-6:ω-3 PUFAs in the non-HDL-C fraction and that the use of the ω-6:ω-3 ratio of PUFAs in serum is a better predictor of coronary heart disease than estimating LDL-C.
on November 12, 2011
at 08:19 PM
I don't think at this point we can be sure that there is a connection between PUFAs and oxLDL. Kismet over at Imminst addressed this issue in a post:http://www.longecity.org/forum/topic/48670-the-oxldlox-stress-pufa-connection-is-very-dubious-evidence/
The issue is that PUFAs could increase oxLDL in the serum because since it is lowering LDL oxLDL particles are being removed from the intimal space. However as I wrote about in my recent blog post (http://hanswuhealth.blogspot.com/2011/11/paleo-folk-beware-of-your-cholesterol.html) it is quite possible that oxLDL may be the instigator, however from then on there the process moves on at a pace determined by many factors (less cases like FH).
If we are arguing on the basis of PUFAs are less stable, thus they COULD cause oxidation in vivo, we don't really know that to be true. By that reasoning, SAFA would be the most stable, however studies comparing the two (albeit limited in number) show that SAFA leads to more oxLDL (possibly inflammatory? discussed here: http://hanswuhealth.blogspot.com/2011/11/lipid-profile-and-goals-part-ii-mufa-vs.html).
While there is lack of data showing the benefit of no PUFAs, there is also lack of data for increased PUFAs, for now I think we can settle down for 20g total a day. 2:1 ratio of w-6:w-3.
on September 09, 2011
at 01:08 AM
High CRP + Plaque = Bad News